The EEPD1 Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the EEPD1 gene has been disrupted through general gene-editing approaches. This product provides a heterogeneous knockout pool derived from the HAP1 host cell line, enabling loss-of-function studies of EEPD1 without monoclonal isolation. The polyclonal format retains the genetic diversity inherent to edited cell populations, making it suitable for robust functional screening and pathway analysis.
HAP1 is a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia (CML) clone, originating from a male patient in blast crisis. Its haploid karyotype (except for chromosome 8) simplifies genetic manipulation, as a single targeting event can produce a complete loss-of-function allele. Widely employed as a versatile platform for haploid genetic screens and cancer model systems, HAP1 cells maintain key signaling pathways relevant to leukemogenesis and DNA damage responses.
The EEPD1 protein is a crucial mediator of DNA end resection during homologous recombination repair. EEPD1 is activated upstream by the ATM kinase in response to DNA double-strand breaks, and it physically interacts with the MRN complex (MRE11?CRAD50?CNBS1) as well as with EXO1 exonuclease and BLM helicase. Mechanistically, EEPD1 promotes the resection of DNA ends by stimulating EXO1 and BLM activities, generating 3′ single-stranded DNA (ssDNA) tails that are rapidly coated by RPA. In the canonical homologous recombination pathway, RPA is subsequently replaced by RAD51 with the assistance of BRCA1 and BRCA2, facilitating homology search and strand invasion. Thus, EEPD1 functions downstream of ATM and CtIP but upstream of RPA?CRAD51 filament formation, positioning it at a pivotal node in the DNA damage response network.
In the context of HAP1 cells, which originate from a CML blast crisis, disruption of EEPD1 impairs homologous recombination repair, potentially sensitizing cells to DNA-damaging agents and revealing synthetic lethal interactions. Given the leukemic background, this knockout model is particularly relevant for studying genomic instability syndromes and for evaluating therapeutic strategies that exploit DNA repair deficiencies. The polyclonal knockout pool allows the study of population-level responses to genotoxic stress without clonal selection bias.
This product is designed for a broad range of research applications, including DNA repair pathway analysis, synthetic lethality screening, and cancer drug response profiling. Representative assays include Western blotting for protein expression, immunofluorescence detection of ??H2AX foci, comet assays for DNA damage, homologous recombination reporter assays, PARP inhibitor sensitivity assays, RNA sequencing, and cell cycle analysis. These EEPD1 Knockout HAP1 Polyclonal Cells serve as a valuable tool for dissecting the molecular mechanisms of DNA end resection and for identifying vulnerabilities in cancer cells. For additional information, please contact Ascent Research.
